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virulence, detoxification, adaptation
information pathways
cell wall and cell processes
stable RNAs
insertion seqs and phages
PE/PPE
intermediary metabolism and respiration
unknown
regulatory proteins
conserved hypotheticals
lipid metabolism
pseudogenes
General annotation
TypeCDS
FunctionRegulator part of the two component regulatory system DEVR/DEVS/dost. Controls HSPX|Rv2031|ACR expression.
ProductTwo component transcriptional regulatory protein DevR (probably LuxR/UhpA-family)
CommentsRv3133c, (MTCY03A2.25), len: 217 aa. DevR (alternate gene name: dosR), two component transcriptional regulator (see Dasgupta et al., 2000; dev for Differentially Expressed in Virulent strain), highly similar to several e.g. O85372|CPRR two component regulator from Rhodococcus sp. (212 aa), FASTA scores: opt: 868, E(): 6.2e-46, (65.05% identity in 206 aa overlap); Q9RI42|SCJ12.16c putative LuxR family two-component response regulator from Streptomyces coelicolor (233 aa), FASTA scores: opt: 849, E(): 9.7e-45, (60.55% identity in 218 aa overlap); Q9XA59|SCGD3.19 putative two-component system response transcriptional regulator from Streptomyces coelicolor (218 aa), FASTA scores: opt: 835, E(): 6.5e-44, (61.55% identity in 208 aa overlap); and similar to others. Contains bacterial regulatory proteins, LuxR family signature (PS00622) near C-terminus as seen in bvgA, comA, dctR, degU, evgA, fimZ, fixJ, gacA, glpR, narL, narP, nodW, rcsB and uhpA. Helix-turn-helix motif at 166-187 (+3.15 SD). Belongs to the LuxR/UhpA family of transcriptional regulators. The N-terminal region is similar to that of other regulatory components of sensory transduction systems.
Functional categoryRegulatory proteins
ProteomicsThe product of this CDS corresponds to spot 3_305 identified in culture supernatant by proteomics at the Max Planck Institute for Infection Biology, Berlin, Germany, and also at the Statens Serum Institute (Denmark) (see proteomics citations). Identified in the membrane fraction of M. tuberculosis H37Rv using 1D-SDS-PAGE and uLC-MS/MS (See Gu et al., 2003). Identified in the culture supernatant of M. tuberculosis H37Rv using mass spectrometry (See Mattow et al., 2003). Identified in the cytosol and cell membrane fraction of M. tuberculosis H37Rv using 2DLC/MS (See Mawuenyega et al., 2005). Identified in the membrane fraction of M. tuberculosis H37Rv using nanoLC-MS/MS (See Xiong et al., 2005). Identified by mass spectrometry in Triton X-114 extracts of M. tuberculosis H37Rv (See Malen et al., 2010). Identified by mass spectrometry in the membrane protein fraction and whole cell lysates of M. tuberculosis H37Rv but not the culture filtrate (See de Souza et al., 2011).
TranscriptomicsmRNA identified by DNA microarray analysis: gene induced by hypoxia (see Sherman et al., 2001), under microaerobic and anaerobic conditions (see Mayuri et al., 2002), and down-regulated after 4h of starvation (see Betts et al., 2002).
MutantNon-essential gene for in vitro growth of H37Rv in a MtbYM rich medium, by Himar1 transposon mutagenesis (see Minato et al. 2019). Non-essential gene for in vitro growth of H37Rv, by analysis of saturated Himar1 transposon libraries (see DeJesus et al. 2017). Non essential gene by Himar1 transposon mutagenesis in H37Rv strain (see Sassetti et al., 2003). Non-essential gene for in vitro growth of H37Rv, by Himar1 transposon mutagenesis (See Griffin et al., 2011). M. tuberculosis H37Rv mutant is attenuated in guinea pigs (See Malhotra et al., 2004). M. tuberculosis H37Rv mutant shows increased virulence in SCID mice; mutant grows more quickly in DBA mice and in IFN-gamma activated macrophages (See Parish et al., 2004).
Check for mutants available at TARGET website
Coordinates
TypeStartEndOrientation
CDS34992623499915-
Genomic sequence
Feature type Upstream flanking region (bp) Downstream flanking region (bp) Update
       
Protein sequence
>Mycobacterium tuberculosis H37Rv|Rv3133c|devR
VVKVFLVDDHEVVRRGLVDLLGADPELDVVGEAGSVAEAMARVPAARPDVAVLDVRLPDGNGIELCRDLLSRMPDLRCLILTSYTSDEAMLDAILAGASGYVVKDIKGMELARAVKDVGAGRSLLDNRAAAALMAKLRGAAEKQDPLSGLTDQERTLLGLLSEGLTNKQIADRMFLAEKTVKNYVSRLLAKLGMERRTQAAVFATELKRSRPPGDGP
      
Bibliography